Alzheimers disease and glycolysis

[jim mcnamara]

NIH news release:
https://www.nih.gov/news-events/new...lucose-levels-may-mean-more-severe-alzheimers

To start with, this does NOT prove a link between glucose blood levels and Alzheimers onset. Or more simply put, this paper does not say: sugar causes Alzheimers. Why did I say this? Popular science writers may inadvertently provide the wrong message. It has happened before.

It shows that for parts of the brain with AZ plaques, severity of plaques has a relationship to the apparent impairment of the glycolytic pathway. More severe plaques in an area == higher glucose levels. And also levels of indicator amino acids to assess glycolysis rates, which appear to be lower. This means that breakdown of glucose is slower than elsewhere in brain tissue. The link has details.

I cannot get to an original paper, @Ygggdrasil may be able to locate something and provide better information.

 

[Ygggdrasil]

Here's a citation for the study:
An et al. 2017 Evidence for brain glucose dysregulation in Alzheimer's disease. Alzheimers Dement. Published online 19 Oct 2017. doi:10.1016/j.jalz.2017.09.011

Abstract:

Introduction
It is unclear whether abnormalities in brain glucose homeostasis are associated with http://www.sciencedirect.com/topics/neuroscience/alzheimers-disease (AD) pathogenesis.

Methods
Within the autopsy cohort of the Baltimore Longitudinal Study of Aging, we measured brain glucose concentration and assessed the ratios of the glycolytic amino acids, serine, glycine, and alanine to glucose. We also quantified protein levels of the neuronal (GLUT3) and astrocytic (GLUT1) glucose transporters. Finally, we assessed the relationships between plasma glucose measured before death and brain tissue glucose.

Results
Higher brain tissue glucose concentration, reduced glycolytic flux, and lower GLUT3 are related to severity of AD pathology and the expression of AD symptoms. Longitudinal increases in fasting plasma glucose levels are associated with higher brain tissue glucose concentrations.

Discussion
Impaired glucose metabolism due to reduced glycolytic flux may be intrinsic to AD pathogenesis. Abnormalities in brain glucose homeostasis may begin several years before the onset of clinical symptoms.

The study shows an association between glucose dysregulation and Alzheimer's disease, but the study cannot assess causation. In my opinion, it seems more likely that Alzheimers' disease would cause dysregulation of glucose metabolism in the affected tissues that the other way around.